Protecting Ribosome Genes May Avoid aging

In the absence of SIRT7, a human primary cell displays multiple nucleoli. DNA was stained with DAPI (turquoise) and nucleolus was stained with anti-fibrillarin (red). Credit- Silvana Paredes

Aging is the process which makes you older with the time and the rate of aging to a large extent is genetically based. With aging, weakening begins inside every cell.

A new research led by the team of researchers from Stanford University and the VA Palo Alto Health Care System (VAPAHCS) have found a protein which protects the cells from age-related problems. These age-related problems are often called senescence. This protein protects the particular vulnerable set of genes which regulates aging.

Ribosomes are the complex molecular machine for synthesizing proteins. Genes encoding ribosome components are present abundantly and are used continuously. Sometimes the active ribosomal genes can get damaged hence many copies of ribosomal genes i.e ribosomal DNA are kept silent. This is important because rDNA is essential but unstable – prone to mutation and rearrangement.

“Ribosomal DNA is one of the major hotspots for instability in the genome,” said Silvana Paredes, the research scientist who led the study.

During their research, scientist investigated the link between rDNA, aging and protein SIRT7. The function of SIRT7 is to modify the protein around which DNA is spiraled and also regulates the gene by turning it off and on. Paredes found that SIRT7 was important for keeping parts of the rDNA turned off. This function turned out to be crucial for preventing aging-related deterioration in the cell.

In the laboratory, the researchers removed the SIRT7 genes in the mice and observed that the cell division was arrested and symptoms of damage and age were also noticed. Such senescent cells accumulate in tissues in aging-related conditions as diverse as cancer, diabetes, heart disease, arthritis, and neurodegeneration. Studies in mice have suggested that removing senescent cells can prevent some of these conditions. Identifying SIRT7 as a protein that keeps cells healthy could, therefore, lead to therapies that prevent cellular senescence.

“By identifying rDNA instability as an underlying trigger of senescence of human cells and demonstrating the central role of SIRT7 in protecting against this process, our studies not only provide important insights into basic mechanisms of aging but also identify potential molecular targets for aging-related disease processes,” Chua said.

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